Delayed cerebral ischemia causing cortical blindness due to repeat cocaine use weeks subsequent to aneurysmal subarachnoid hemorrhage

Abstract

Cocaine is a known vasoactive drug associated with poor clinical outcomes and high in-hospital mortality related to aneurysmal subarachnoid hemorrhage; however, the association of prior cocaine use with the incidence of vasospasm and delayed cerebral ischemia remains controversial. We report a case of a 42-year-old male with a history of active cocaine use who presented with a severe headache. Imaging demonstrated diffuse cisternal subarachnoid hemorrhage due to a ruptured basilar apex aneurysm, which was successfully treated with endovascular coil embolization. Despite expedited endovascular treatment and an initially benign clinical course, he suffered from delayed cerebral ischemia resulting in cortical blindness due to bilateral posterior cerebral artery vasospasm secondary to repeat cocaine use weeks after his initial ictus. To our knowledge, the present case is the first to describe delayed cerebral ischemia resulting in a severe neurologic deficit due to repeat cocaine use weeks subsequent to aneurysm rupture. We review the current literature on the association of cocaine use with the incidence of vasospasm and delayed cerebral ischemia as well as the effects of cocaine on the cerebrovasculature.

Keywords: Aneurysm; CT, computed tomography; CTA, computed tomography angiography; DCI, delayed cerebral ischemia; TCD, transcranial Doppler; cocaine; delayed cerebral ischemia; subarachnoid hemorrhage; vasospasm.

Fig. 1

Imaging on presentation. (A) Axial CT demonstrated thick diffuse cisternal subarachnoid hemorrhage with clot within the interpeduncular cistern. (B) Axial and (C) coronal CT angiography revealed a large irregular saccular aneurysm arising from the basilar artery apex eccentric to the right.

Fig. 2

Digital subtraction angiography of a right vertebral artery injection pre- and postembolization revealed a 4.0 × 4.4 mm saccular aneurysm projecting eccentrically to the right from the basilar artery apex and small daughter sac projecting anterior-superior. (A) Anterior-posterior and (B) lateral views pre-embolization. (C) Anterior-posterior and (D) lateral views postembolization. (E) and (F) Digital subtraction angiography of a right internal carotid artery injection, which demonstrated diffuse small caliber cerebrovasculature and a fetal posterior-communicating artery.

Fig. 3

Imaging on representation on post-procedure day 17. (A) Axial CT revealed extensive ischemic infarction of the bilateral posterior cerebral artery distributions. (B) Digital subtraction angiography of a right vertebral artery injection anterior-posterior view with severe P2/3 junction vasospasm and sluggish flow through multiple P4 segments. (C) Right internal carotid artery injection lateral view with severe vasospasm involving the near fetal-type posterior communicating artery and diminutive flow through the posterior cerebral artery distributions.